Hepatoprotective Activity of Ligustilide Against Acetaminophen-induced Acute Liver Toxicity in Rats via Inhibiting Oxidative Stress and Inflammatory Responses

Background: Drug-induced liver toxicity is a major clinical challenge, being the primary cause of abrupt liver failure. This condition is intensified by an older population that consumes more drugs and the increasing hazards associated with unknown drug consumption. Objectives: This work was undertaken to study the beneficial values of ligustilide against acetaminophen-induced liver damage in rats. Materials and Methods: The experimental rats were administered 640 mg/kg of acetaminophen to induce experimental liver toxicity and successively treated with ligustilide. Upon concluding the treatments, the concentrations of liver function marker enzyme activities, albumin, protein, and total/direct bilirubin were assessed using respective test kits. The concentrations of antioxidants, inflammatory cytokines, and lipid profile markers were assessed using the commercial test kits. The liver tissues acquired from the experimental rats were employed for a histological study. Results: The ligustilide treatment significantly normalized the changes in hepatic function marker enzymes, elevated albumin and protein concentrations, and reduced total/direct bilirubin contents in the rats with acetaminophen-induced hepatic toxicity. Furthermore, the ligustilide treatment resulted in increased antioxidant concentrations and significantly decreased inflammatory cytokine levels. In addition, the ligustilide considerably mitigated the dyslipidemia condition in the experimental rats. The outcomes of the histological study of hepatic tissues further confirmed the hepatoprotective efficacy of ligustilide. Conclusion: The findings of this work demonstrate the hepatoprotective effects of ligustilide against acetaminophen-induced liver toxicity in rats. Consequently, ligustilide can serve as a viable treatment option for addressing drug-induced liver toxicity.